Ben H Jansen1, Lingli Hu, Nash N Boutros. 1. Department of Electrical and Computer Engineering, and Center for Neuro-Engineering and Cognitive Science, University of Houston, TX 77204-4005, United States. bjansen@uh.edu
Abstract
OBJECTIVES: To investigate if the reduced P50, N100 and P200 auditory evoked potential (EP) components and gating deficits seen in schizophrenia can be explained in terms of response incompleteness. METHODS: Twenty-five healthy and schizophrenia participants were studied using pairs of 1000Hz tones (S1 and S2, 0.5s apart) separated by 8.0s. A correlation-based clustering method identified the responses containing P50, N100, and/or P200 related-activity. RESULTS: Schizophrenia participants produced fewer S1 and S2 responses containing all three EP components than healthy participants. Healthy participants, but not the patient population, produced fewer and smaller S2 than S1 responses containing all three EP components. However, the S2 responses following complete S1 responses were smaller than the complete S1 responses in both populations. CONCLUSIONS: The gating deficits observed in schizophrenia are due to two mechanisms. First, the S1 response consistency is less in schizophrenia than in health. Second, the S2 responses are attenuated less in schizophrenia. SIGNIFICANCE: This research contributes to the understanding of response variability and sensory gating in health and schizophrenia. It also extends previous reports that fewer and smaller P300 components are produced in schizophrenia than in health to the mid-latency component range. Copyright 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
OBJECTIVES: To investigate if the reduced P50, N100 and P200 auditory evoked potential (EP) components and gating deficits seen in schizophrenia can be explained in terms of response incompleteness. METHODS: Twenty-five healthy and schizophreniaparticipants were studied using pairs of 1000Hz tones (S1 and S2, 0.5s apart) separated by 8.0s. A correlation-based clustering method identified the responses containing P50, N100, and/or P200 related-activity. RESULTS:Schizophreniaparticipants produced fewer S1 and S2 responses containing all three EP components than healthy participants. Healthy participants, but not the patient population, produced fewer and smaller S2 than S1 responses containing all three EP components. However, the S2 responses following complete S1 responses were smaller than the complete S1 responses in both populations. CONCLUSIONS: The gating deficits observed in schizophrenia are due to two mechanisms. First, the S1 response consistency is less in schizophrenia than in health. Second, the S2 responses are attenuated less in schizophrenia. SIGNIFICANCE: This research contributes to the understanding of response variability and sensory gating in health and schizophrenia. It also extends previous reports that fewer and smaller P300 components are produced in schizophrenia than in health to the mid-latency component range. Copyright 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
Authors: Robert E Lin; Lauren Ambler; Eddie N Billingslea; Jimmy Suh; Shweta Batheja; Valerie Tatard-Leitman; Robert E Featherstone; Steven J Siegel Journal: Physiol Rep Date: 2013-10-20
Authors: Kyung Soon Shin; June Sic Kim; Sung Nyun Kim; Kyung Sue Hong; Brian F O'Donnell; Chun Kee Chung; Jun Soo Kwon Journal: NPJ Schizophr Date: 2015-09-02